By David Haig
A woman who gives birth to six children each with a 75% chance of survival has the same expected number of surviving offspring as a woman who gives birth to five children each with a 90% chance of survival. In both cases, 4.5 offspring are expected to survive. Because the large fitness gain from an additional child can compensate for a substantially increased risk of childhood mortality, women’s bodies will have evolved to produce children closer together than is best for child fitness.
Sleeping baby by Minoru Nitta. CC BY 2.0 via Flickr.
Offspring will benefit from greater birth-spacing than maximizes maternal fitness. Therefore, infants would benefit from adaptations for delaying the birth of a younger sib. The increased risk of mortality from close spacing of births is experienced by both the older and younger child whose births bracket the interbirth interval. Although a younger sib can do nothing to cause the earlier birth of an older sib, an older sib could potentially enhance its own survival by delaying the birth of a younger brother or sister.
The major determinant of birth-spacing, in the absence of contraception, is the duration of post-partum infertility (i.e., how long after a birth before a woman resumes ovulation). A woman’s return to fertility appears to be determined by her energy status. Lactation is energetically demanding and more intense suckling by an infant is one way that an infant could potentially influence the timing of its mother’s return to fertility. In 1987, Blurton Jones and da Costa proposed that night-waking by infants enhanced child survival not only because of the nutritional benefits of suckling but also because of suckling’s contraceptive effects of delaying the birth of a younger sib.
Blurton Jones and da Costa’s hypothesis receives unanticipated support from the behavior of infants with deletions of a cluster of imprinted genes on human chromosome 15. The deletion occurs on the paternally-derived chromosome in Prader-Willi syndrome (PWS). Infants with PWS have weak cries, a weak or absent suckling reflex, and sleep a lot. The deletion occurs on the maternally-derived chromosome in Angelman syndrome (AS). Infants with AS wake frequently during the night.
The contrasting behaviors of infants with PWS and AS suggest that maternal and paternal genes from this chromosome region have antagonistic effects on infant sleep with genes of paternal origin (absent in PWS) promoting suckling and night waking whereas genes of maternal origin (absent in AS) promote infant sleep. Antagonistic effects of imprinted genes are expected when a behavior benefits the infant’s fitness at a cost to its mother’s fitness with genes of paternal origin favoring greater benefits to infants than genes of maternal origin. Thus, the phenotypes of PWS and AS suggest that night waking enhances infant fitness at a cost to maternal fitness. The most plausible interpretation is that these costs and benefits are mediated by effects on the interbirth interval.
Postnatal conflict between mothers and offspring has been traditionally assumed to involve behavioral interactions such as weaning conflicts. However, we now know that a mother’s body is colonized by fetal cells during pregnancy and that these cells can persist for the remainder of the mother’s life. These cells could potentially influence interbirth intervals in more direct ways. Two possibilities suggest themselves. First, offspring cells could directly influence the supply of milk to their child, perhaps by promoting greater differentiation of milk-producing cells (mammary epithelium). Second, offspring cells could interfere with the implantation of subsequent embryos. Both of these possibilities remain hypothetical but cells containing Y chromosomes (presumably derived from male fetuses) have been found in breast tissue and in the uterine lining of non-pregnant women.
David Haig is Professor of Biology at Harvard University. he is the author of “Troubled sleep: Night waking, breastfeeding and parent–offspring conflict” (available to read for free for a limited time) in Evolution, Medicine, and Public Health. The arguments summarized above are presented in greater detail in two papers that recently appeared in Evolution, Medicine, and Public Health.
Evolution, Medicine, and Public Health is an open access journal, published by Oxford University Press, which publishes original, rigorous applications of evolutionary thought to issues in medicine and public health. It aims to connect evolutionary biology with the health sciences to produce insights that may reduce suffering and save lives. Because evolutionary biology is a basic science that reaches across many disciplines, this journal is open to contributions on a broad range of topics, including relevant work on non-model organisms and insights that arise from both research and practice.
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Over the past year, the SciWhys column has explored a number of different topics, from our immune system to plants, from viruses to DNA. But why is an understanding of topics such as these so important? In short, using science to understand our world can help to improve our lives. In this post and the next, I want to illustrate this point with an example of how progress in science is providing hope for the future for one family, and many others like them.
By Jonathan Crowe
Carys is an angelic-looking two-year old, with a truly winning smile. At first sight, then, she seems no different from any other child her age. Yet Carys’ smile belies a heart-rending reality: Carys has Rett syndrome, a disorder of the nervous system that is as widespread in the population as cystic fibrosis, yet is recognised to only a fraction of the same extent. (I, for one, had never heard of it until just a few months ago.)
Rett syndrome is a delayed onset disorder — something whose effects only become apparent with time. When Carys was born, she appeared perfectly healthy, and developed in much the same way as any other healthy infant. Just as she began to master her first few words, however, she lost the power of speech, and soon lost the use of her hands too. The effects of Rett syndrome were beginning to be felt.
Over time, Rett syndrome robs young girls of their motor control: they lose the ability to walk, to hold or carry objects, and to speak. But there be other complications too: there may be digestive problems; difficulties eating, chewing, and swallowing; and seizures and tremors. It is a truly debilitating disorder.
So what causes Rett syndrome? What’s happened inside the body of young girls like Carys? We know that the syndrome is caused by as little as a single error (a mutation) in a single gene. (As I mention in a previous post, it’s quite unsettling to realise that just one error in the tens of millions of letters that spell out the sequence of our genomes is sufficient to cause certain diseases. Sometimes there’s very little room for error.) The normal, healthy gene (called MECP2) contains the instructions for the cell to manufacture a particular protein; the mutated gene produces a broken form of this protein, which no longer functions as it should.
But how can a single protein affect so many processes – from speech to the movement of limbs? The answer lies in the way the protein interacts with other genes, particularly in brain cells. Essentially, the protein acts like a cellular librarian by helping the cells in the brain to make use of the information stored in their genomes (their libraries of genes). If the protein is broken, the cells can no longer make use of all of the genetic information needed for them to work properly (a bit like trying to use an instruction manual with some of the pages blacked out), so normal processes begin to break down. The broken protein doesn’t just affect the ability of the brain cells to use one or two other genes, but a whole range of them – and that’s why the effects of Rett syndrome are so wide-ranging.
But the story of Rett syndrome runs deeper than this. The mutation that causes Rett syndrome occurs in sperm; it happens after the sp
By: Lauren,
on 5/31/2011
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By Allen J. Wilcox
On making boy babies, and other pregnancy myths
In her novel, Prodigal Summer, Barbara Kingsolver celebrates the lush fecundity of nature. The main character marvels at the way her ovulation dependably comes with the full moon.
It’s a poetic image – but is there any evidence for it?
Actually, no. It’s true that the length of the average menstrual cycle is close to the length of the lunar cycle. But like so many notions about fertility, an effect of the moon on ovulation is just a nice story. The menstrual cycle is remarkably variable, even among women who say their cycles are “regular.” This is not surprising – unlike the movement of stars and planets, biology is full of variation. The day of ovulation is unpredictable, and there is no evidence (even in remote tribal cultures) that ovulation is related to phases of the moon or other outside events.
We humans are susceptible to myths about our fertility and pregnancy. These myths also invade science. One scientific “fact” you may have heard is that women who live in close quarters synchronize their menstrual cycles. The paper that launched this idea was published forty years ago in the prestigious journal Nature1. Efforts to replicate those findings have been wobbly at best – but the idea still persists.
Another scientific myth is the notion that sperm carrying the Y male chromosome swim faster than sperm carrying the X female chromosome. It’s true that the Y chromosome is smaller than the X. But there is no evidence that this very small addition of genetic cargo slows down the X-carrying sperm. As often as this idea is debunked, it continues to appear in scientific literature – and especially the literature suggesting that couples can tilt the odds towards having a baby of a particular sex.
Choosing your baby’s sex
Many couples have a definite preference for the sex of their baby. The baby’s sex is established at conception, which has led to a lot of advice on things to do around the time of conception to favor one sex or the other. Recommendations include advice on timing of sex in relation to ovulation, position during sex, frequency of sex, foods to eat or avoid, etc. The good thing about every one of these techniques is that they work 50% of the time. (This is good enough to produce many sincere on-line testimonials.) Despite what you may read, there is no scientific evidence that any of these methods improves your chances for one sex or the other, even slightly. The solution? Relax and enjoy what you get.
When will the baby arrive?
Everyone knows that pregnancies last nine months – but do they? Doctors routinely assign pregnant women a “due-date,” estimated from the day of her last menstrual period before getting pregnant. The due-date is set at 40 weeks after the last menstrual period. You might think the due-date is based on scientific evidence, but in fact, 40 weeks was proposed in 1709 for a rather flaky reason: since the average menstrual period is four weeks, it seemed “harmonious” for pregnancy to last the equivalent of ten menstrual cycles.
So what are a woman’s chances of actually delivering on her due date? Fifty percent? Twenty percent?
Try four percent. Just like the length of menstrual cycles (and every other aspect of human biology), there is lots of variation in the natural length of pregnancy. If the due-date is useful at all, it is as the median length of pregnancy – in other words, about half of women will deliver before their due-date, and about half after. So don’t cancel your appointments on the due-date just because you think it’s The Day – there’s a 96% chance the baby will arrive some other time.
1. McClintock MK. Menstrual synchorony and suppression.
By: Kirsty,
on 3/28/2011
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This is the second post in our latest regular OUPblog column: SciWhys. Every month OUP editor and author Jonathan Crowe will be answering your science questions. Got a burning question about science that you’d like answered? Just email it to us, and Jonathan will answer what he can. Today: What are genes and genomes?
By Jonathan Crowe
I described in my last blog post how DNA acts as a store of biological information – information that serves as a set of instructions that direct our growth and function. Indeed, we could consider DNA to be the biological equivalent of a library – another repository of information with which we’re all probably much more familiar. The information we find in a library isn’t present in one huge tome, however. Rather, it is divided into discrete packages of information – namely books. And so it is with DNA: the biological information it stores isn’t captured in a single, huge molecule, but is divided into separate entities called chromosomes – the biological equivalent of individual books in a library.
I commented previously that DNA is composed of a long chain of four building blocks, A, C, G, and T. Rather than existing as an extended chain (like a stretched out length of rope), the DNA in a chromosome is tightly packaged. In fact, if stretched out (like our piece of rope), the DNA in a single chromosome would be around 2-8 cm long. Yet a typical chromosome is just 0.00002–0.002 cm long: that’s between 1000 and 100,000 times shorter than the unpackaged DNA would be. This packaging is quite the feat of space-saving efficiency.
Let’s return to our imaginary library of books. The information in a book isn’t presented as one long uninterrupted sequence of words. Rather, the information is divided into chapters. When we want to find out something from a book – to extract some specific information from it – we don’t read the whole thing cover-to-cover. Instead, we may just read a single chapter. In a fortuitous extension of our analogy, the same is true of information retrieval from chromosomes. The information captured in a single chromosome is stored in discrete ‘chunks’ (just as a book is divided into chapters), and these chunks can be read separately from one another. These ‘chunks’ – these discrete units of information – are what we call ‘genes’. In essence, one gene contains one snippet of biological information.
I’ve just likened chromosomes to books in a library. But is there a biological equivalent of the library itself? Well, yes, there is. Virtually every cell in the human body (with specific exceptions) contains 46 chromosomes – 23 from each of its parents. All of the genes found in this ‘library’ of chromosomes are collectively termed the ‘genome’. Put another way, a genome is a collection of all the genes found in a particular organism.
Different organisms have different-sized genomes. For example, the human genome comprises around 20,000-25,000 genes; the mouse genome, with 40 chromosomes, comprises a similar number of individual genes. However, the bacterium H. influenzae has just a single chromosome, containing around 1700 genes.
It is not just the number of genes (and chromosomes) in the genome that varies between organisms: the long stretches of DNA making up the genomes of different organisms have different sequences (and so store different information). These differences make sense, particularly if we imagine the genome of an organism to represent the ‘recipe’ for that organism: a human is quite a different organism from a mouse, so we would expect the instructions that direct the growth and function of the two organisms to differ.
B
